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Do we know what causes prostate cancer?

We do not know exactly what causes prostate cancer. But researchers have found some risk factors and are trying to learn just how these factors cause prostate cells to become cancerous (see section “What are the risk factors for prostate cancer?”).

On a basic level, prostate cancer is caused by changes in the DNA of a prostate cell. Scientists have made great progress in understanding how certain changes in DNA can make normal prostate cells grow abnormally and form cancers. DNA is the chemical in each of our cells that makes up our genes, the instructions for nearly everything our cells do. We usually look like our parents because they are the source of our DNA. However, DNA affects more than how we look.

Some genes control when our cells grow, divide into new cells, and die. Certain genes that help cells grow, divide, and stay alive are called oncogenes. Others that normally slow down cell division, repair mistakes in DNA, or cause cells to die at the right time are called tumor suppressor genes. Cancer can be caused in part by DNA changes (mutations) that turn on oncogenes or turn off tumor suppressor genes.

DNA changes can either be inherited from a parent or can be acquired during a person’s lifetime.

Inherited DNA mutations

Inherited DNA changes in certain genes seem to cause about 5% to 10% of prostate cancers. Several mutated genes have been linked to a man’s inherited tendency to develop prostate cancer, including:

RNASEL (formerly HPC1): The normal function of this tumor suppressor gene is to help cells die when something goes wrong inside them. Inherited mutations in this gene might let abnormal cells live longer than they should, which can lead to an increased risk of prostate cancer.

BRCA1 and BRCA2: These tumor suppressor genes normally help repair mistakes in a cell’s DNA (or cause the cell to die if the mistake can’t be fixed). Inherited mutations in these genes more commonly cause breast and ovarian cancer in women. But inherited BRCA changes also account for a very small number of prostate cancers.

DNA mismatch repair genes (such as MSH2 and MLH1): These genes normally help fix mistakes (mismatches) in DNA that are made when a cell is preparing to divide into 2 new cells. (Cells must make a new copy of their DNA each time they divide.) Men with inherited mutations in these genes have a condition known as Lynch syndrome, and are at increased risk of colorectal, prostate, and some other cancers.

Other inherited gene mutations may account for some cases of hereditary prostate cancer, although none of these is a major cause. More research is being done on these genes.

DNA mutations acquired during a man’s lifetime

Most DNA mutations related to prostate cancer seem to develop during a man’s life rather than having been inherited.

Every time a cell prepares to divide into 2 new cells, it must copy its DNA. This process is not perfect, and sometimes errors occur, leaving flawed DNA in the new cell. It is not clear how often these DNA changes might be random events, and how often they are influenced by other factors (diet, hormone levels, etc.). In general, the more quickly prostate cells grow and divide, the more chances there are for mutations to occur. Therefore, anything that speeds up this process may make prostate cancer more likely.

The development of prostate cancer may be linked to increased levels of certain hormones. High levels of androgens (male hormones, such as testosterone) promote prostate cell growth, and might contribute to prostate cancer risk in some men.

Some researchers have noted that men with high levels of another hormone, insulin-like growth factor-1 (IGF-1), are more likely to get prostate cancer. IGF-1 is similar to insulin, but it affects cell growth, not sugar metabolism. However, other studies have not found a link between IGF-1 and prostate cancer. Further research is needed to make sense of these findings.

As mentioned in the “What are the risk factors for prostate cancer?” section, some studies have found that inflammation in the prostate may contribute to prostate cancer. One theory is that inflammation might lead to cell DNA damage, which might in turn push a cell closer to becoming cancerous. More research in this area is needed.

Exposure to radiation or cancer-causing chemicals can cause DNA mutations in many organs, but these factors have not been proven to be important causes of mutations in prostate cells.